Abstract: The dose rate with which radiation is delivered significantly affects the biological response to radiation and reducing the dose rate decreases the biological effect. However, DNA damage introduced at a reduced rate does not activate the DNA damage sensor ATM and that failure to activate ATM-associated repair pathways contributes to the increased lethality of continuous radiation exposures, which has been termed the "inverse dose rate effect". Under continuous low dose rate irradiation, there are two major pathways by which DSB's can be repaired, nonhomologous end joining (NHEJ), and homologous recombination(HR), which play an important role in sublethal damage repair and the generation of dose-rate effect. A change in sensitivity is modified if DNA damage can be repaired with high fidelity. The cells will lead to apoptosis if the cell DNA damage is not sufficiently repaired. The p53 gene is a key factor in the radiation-induced the cell cycle arrest and the activation of apoptosis after exposure to low dose-rate irradiation.